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Chris Etheridge PhD MCPP (Medical Herbalist) - …

The seedling growth inhibitors include the following herbicide families: dinitroanilines, acetanilides, and thiocarbamates. Seedling growth inhibitors interfere with new plant growth, thereby reducing the ability of seedlings to develop normally in the soil. Herbicides in these families must be soil-applied. Plants can take up these herbicides after germinating until the seedling emerges from the soil. Therefore, these herbicides are only effective on seedling annual or perennial weeds. Plants that have emerged from the soil uninjured are likely to remain unaffected. Seedling growth inhibitors are active at two main sites, the developing shoot and the root. Much more is known about how seedling root inhibiting herbicides work than about how seedling shoot inhibitors work. The root inhibitors stop plant cells from dividing, which inhibits shoot elongation and lateral root formation. Uptake is through developing roots and shoots. Because herbicide movement within the plant is limited, herbicide injury is confined primarily to plant roots and shoots. Shoot inhibiting herbicides are taken up by developing roots and shoots and can move via the xylem to areas of new growth. There is evidence to suggest that these herbicides can affect multiple sites within a plant, primarily interfering with lipid and protein synthesis.

Chris Etheridge’s qualifications, experience and publications
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Simple derivatives such as methcathinone and -dimethylcathinone can be synthesised by oxidation of ephedrine (or pseudoephedrine) and-methylephedrine (or -methylpseudoephedrine) respectively. This requires reacting the precursor with a solution of potassium permanganate in dilute sulfuric acid. The precursors can be obtained as specific enantiomers, thereby ensuring that the synthesis is stereoselective. Cathinone itself can be made in a similar way, starting from phenylpropanolamine (norephedrine). One of the hazards of the permanganate process is that users can suffer manganese poisoning if the product is not purified.

Toxicity of 2-methyl-5,6-cyclopentapyrimidine (MCPP) Gerald L

Kennedy Jr; Article first published online: 11 JAN 2006
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Rats were trained to discriminate the 5-HT receptor agonists m-chlorophenylpiperazine (mCPP; 1 mg/kg) from saline using a two-lever, water-reinforced drug discrimination task. The antidepressant trazodone (1-8 mg/kg), the 5-HT1B/2C receptor agonists 1-(m-trifluoromethylphenyl)piperazine (TFMPP; 0.25-1 mg/kg) and MK 212 (0.125-1 mg/kg), and the mixed 5-HT1A/B receptor agonist RU 24969 (0.25-2 mg/kg) substituted fully for mCPP. The 5-HT2A/2C receptor agonists 1-(2,5-dimethoxy-4-iodophenyl) -2-aminopropane (DOI; 0.25-1 mg/kg) and d-lysergic acid diethylamide (LSD; 0.02-0.08 mg/kg) and the 5-HT releaser fenfluramine (0.5-2 mg/kg) also mimicked mCPP. Agonists selective for the 5-HT1A or 5-HT3 receptor or the 5-HT reuptake site produced saline-lever responding. The ergoline derivative mesulergine (0.5-4 mg/kg) produced a partial agonist/antagonist profile. The 5-HT 1 2 receptor antagonist metergoline (0.125-2 mg/kg) completely blocked the mCPP cue whereas the 5-HT2A/2C receptor antagonists ketanserin and LY 53857 as well as all other 5-HT receptor antagonists failed to block the mCPP cue. The dopamine receptor antagonists SCH 23390 and haloperidol were also ineffective mCPP antagonists. Following pretreatment with the 5-HT synthesis inhibitor p-chlorophenylalanine (pCPA; 100 mg/kg/day) for 3 consecutive days, the discriminability of low doses of mCPP increased, whereas the effects of fenfluramine decreased. The present results suggest that the discriminative stimulus effects of mCPP in rats are mediated primarily by postsynaptic 5-HT2C receptors.

N2 - Rats were trained to discriminate the 5-HT receptor agonists m-chlorophenylpiperazine (mCPP; 1 mg/kg) from saline using a two-lever, water-reinforced drug discrimination task. The antidepressant trazodone (1-8 mg/kg), the 5-HT1B/2C receptor agonists 1-(m-trifluoromethylphenyl)piperazine (TFMPP; 0.25-1 mg/kg) and MK 212 (0.125-1 mg/kg), and the mixed 5-HT1A/B receptor agonist RU 24969 (0.25-2 mg/kg) substituted fully for mCPP. The 5-HT2A/2C receptor agonists 1-(2,5-dimethoxy-4-iodophenyl) -2-aminopropane (DOI; 0.25-1 mg/kg) and d-lysergic acid diethylamide (LSD; 0.02-0.08 mg/kg) and the 5-HT releaser fenfluramine (0.5-2 mg/kg) also mimicked mCPP. Agonists selective for the 5-HT1A or 5-HT3 receptor or the 5-HT reuptake site produced saline-lever responding. The ergoline derivative mesulergine (0.5-4 mg/kg) produced a partial agonist/antagonist profile. The 5-HT 1 2 receptor antagonist metergoline (0.125-2 mg/kg) completely blocked the mCPP cue whereas the 5-HT2A/2C receptor antagonists ketanserin and LY 53857 as well as all other 5-HT receptor antagonists failed to block the mCPP cue. The dopamine receptor antagonists SCH 23390 and haloperidol were also ineffective mCPP antagonists. Following pretreatment with the 5-HT synthesis inhibitor p-chlorophenylalanine (pCPA; 100 mg/kg/day) for 3 consecutive days, the discriminability of low doses of mCPP increased, whereas the effects of fenfluramine decreased. The present results suggest that the discriminative stimulus effects of mCPP in rats are mediated primarily by postsynaptic 5-HT2C receptors.

Mecoprop (2-(4-Chloro-2-Methylphenoxy) Propionic …

Mcpp - Buy China Mcpp in EC21 global marketplace
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Synthetic cathinones are related to the parent compound cathinone (Figure 1), one of the psychoactive principals in ( Forsk). Cathinone derivatives are the β-keto (βk) analogues of a corresponding . The group includes several substances that have been used as of medicinal products, e.g. amfepramone (diethylpropion; Figure 2). Since the mid-2000s, unregulated ring-substituted cathinone derivatives have appeared in the European recreational drugs market. The most commonly available cathinones sold on the recreational market in the period up to 2010 appear to be mephedrone (Figure 3) and methylone (Figure 4). These products are usually encountered as highly pure white or brown powders. Ring-substituted cathinone derivatives are claimed to have effects similar to those of , or (ecstasy), but little is known of their detailed pharmacology. Apart from cathinone (Figure 1), methcathinone (Figure 5) and two ’s amfepramone (Figure 2) and pyrovalerone, cathinone derivatives are not under international control.

The growth regulators include the following herbicide families: phenoxy acetic acids, benzoic acids, and the pyridines. Growth regulator herbicides can act at multiple sites in a plant to disrupt hormone balance and protein synthesis and thereby cause a variety of plant growth abnormalities. Growth regulator herbicides selectively kill broadleaf weeds; however, they are capable of injuring grass crops. Herbicides in this group can move in both the xylem and the phloem to areas of new plant growth. As a result, many herbicides in this group are effective on perennial and annual broadleaf weeds. Herbicide uptake is primarily through the foliage but root uptake is possible. Injury symptoms are most obvious on newly developing leaves.

Thai Toray Synthetics Company Limited (TTS) | TORAY
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The amino acid synthesis inhibitors include the following herbicide families: sulfonylureas, imidazolinones, sulfonamide, and amino acid derivatives. Amino acid synthesis inhibitors act on a specific enzyme to prevent the production of specific amino acids, key building blocks for normal plant growth and development. Sulfonylurea, imidazolinone, and sulfonamide herbicides prevent the production of three essential branch-chain amino acids by inhibiting one key plant enzyme. The amino acid derivative herbicides inhibit the production of three essential aromatic amino acids by inhibiting another key plant enzyme. In general, injury symptoms are slow to develop (1 to 2 weeks) and include stunting or slowing of plant growth and a slow plant death. Herbicides in the sulfonylurea, imidazolinone, and sulfonamide families can move in both the xylem and phloem to areas of new growth and can be taken up through plant foliage and roots. Herbicides in these three families may have activity on annual and perennial broadleaf or grass weeds and may be soil- or foliar-applied. The amino acid derivative herbicides are nonselective and the site of uptake is the plant foliage. Herbicides in this family move via the phloem to all parts of the plant; these are excellent perennial weed control herbicides and are active on annual weeds as well.

Herbicide Mode of Action and Injury Symptoms

AB - Rats were trained to discriminate the 5-HT receptor agonists m-chlorophenylpiperazine (mCPP; 1 mg/kg) from saline using a two-lever, water-reinforced drug discrimination task. The antidepressant trazodone (1-8 mg/kg), the 5-HT1B/2C receptor agonists 1-(m-trifluoromethylphenyl)piperazine (TFMPP; 0.25-1 mg/kg) and MK 212 (0.125-1 mg/kg), and the mixed 5-HT1A/B receptor agonist RU 24969 (0.25-2 mg/kg) substituted fully for mCPP. The 5-HT2A/2C receptor agonists 1-(2,5-dimethoxy-4-iodophenyl) -2-aminopropane (DOI; 0.25-1 mg/kg) and d-lysergic acid diethylamide (LSD; 0.02-0.08 mg/kg) and the 5-HT releaser fenfluramine (0.5-2 mg/kg) also mimicked mCPP. Agonists selective for the 5-HT1A or 5-HT3 receptor or the 5-HT reuptake site produced saline-lever responding. The ergoline derivative mesulergine (0.5-4 mg/kg) produced a partial agonist/antagonist profile. The 5-HT 1 2 receptor antagonist metergoline (0.125-2 mg/kg) completely blocked the mCPP cue whereas the 5-HT2A/2C receptor antagonists ketanserin and LY 53857 as well as all other 5-HT receptor antagonists failed to block the mCPP cue. The dopamine receptor antagonists SCH 23390 and haloperidol were also ineffective mCPP antagonists. Following pretreatment with the 5-HT synthesis inhibitor p-chlorophenylalanine (pCPA; 100 mg/kg/day) for 3 consecutive days, the discriminability of low doses of mCPP increased, whereas the effects of fenfluramine decreased. The present results suggest that the discriminative stimulus effects of mCPP in rats are mediated primarily by postsynaptic 5-HT2C receptors.

These seven major modes of action are as follows: growth regulation, amino acid synthesis inhibition, ..

The photosynthesis inhibitors include the following herbicide families: triazines, phenylureas, uracils, benzothiadiazoles, and nitriles. Photosynthesis inhibitors shut down the photosynthetic (food producing) process in susceptible plants by binding to specific sites within the plant's chloroplasts. Inhibition of photosynthesis could result in a slow starvation of the plant; however, the plant experiences a more rapid death that is believed to be due to the production of secondary toxic substances. Injury symptoms include yellowing (chlorosis) of leaf tissue followed by death (necrosis) of the tissue. Three of the herbicide families (triazines, phenylureas, and uracils) are taken up into the plant via the roots or foliage and move in the xylem to plant leaves. As a result, injury symptoms will first appear on the older leaves, along the leaf margin. After foliar application, triazine, phenylurea, and uracil herbicides are less mobile and do not move out of the leaf tissue. The nitrile and benzothiadiazole herbicide families are not mobile in plants and are classified as postemergence contact herbicides. These herbicides have no soil activity. Contact herbicides must thoroughly cover a susceptible plant's foliage if complete control is to be achieved. Photosynthetic inhibitors may control annual or perennial grass or broadleaf weeds.

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